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Overview of the postulated mechanisms linking cancer and thrombosis.
Pathophysiol Haemost Thromb. 2008; 36(3-4):122-30.PH

Abstract

Blood coagulation appears to play an important role in the occurrence of cancer and its effects may be twofold. First, in patients with cancer, blood coagulation is activated in the direction of a prothrombotic state. Second, a procoagulant environment may promote cancer in different ways. In this chapter we discuss some of the mechanisms that may be involved in this interplay between coagulation and cancer. Blood coagulation proteins interact with cells in the vasculature to maintain hemostasis. However, many proteins that are involved in coagulation and anticoagulation, as well as fibrinolysis, are also found in extravascular tissues. In different organs, these proteins may be involved in cell-signaling mechanisms, through interaction with cell receptors like protease-activated receptors (PARs). Such interactions may drive inflammation, angiogenesis and cell proliferation. The potential procarcinogenic actions of proteases like thrombin may be counteracted by the anticoagulant and anti-inflammatory actions of the protein C-thrombomodulin mechanism. In the blood of cancer patients, the balance is usually shifted towards a procoagulant direction. The resulting excess thrombin- and fibrin-forming activity promotes venous thrombosis and may in the extravascular compartment stimulate cancer progression. The activation of platelets and their interaction with leukocytes may propagate this process. In addition to the therapeutic modulation of the prothrombotic environment, the induction of specific anticoagulant proteins including thrombomodulin may have effects on tumor growth or dissemination, but the nature of these effects still remains hard to predict. The interplay between cancer and blood coagulation merits further experimental and clinical research.

Authors+Show Affiliations

Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands. h.tencate@bioch.unimaas.nlNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19176985

Citation

ten Cate, Hugo, and Anna Falanga. "Overview of the Postulated Mechanisms Linking Cancer and Thrombosis." Pathophysiology of Haemostasis and Thrombosis, vol. 36, no. 3-4, 2008, pp. 122-30.
ten Cate H, Falanga A. Overview of the postulated mechanisms linking cancer and thrombosis. Pathophysiol Haemost Thromb. 2008;36(3-4):122-30.
ten Cate, H., & Falanga, A. (2008). Overview of the postulated mechanisms linking cancer and thrombosis. Pathophysiology of Haemostasis and Thrombosis, 36(3-4), 122-30. https://doi.org/10.1159/000175150
ten Cate H, Falanga A. Overview of the Postulated Mechanisms Linking Cancer and Thrombosis. Pathophysiol Haemost Thromb. 2008;36(3-4):122-30. PubMed PMID: 19176985.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Overview of the postulated mechanisms linking cancer and thrombosis. AU - ten Cate,Hugo, AU - Falanga,Anna, Y1 - 2009/01/27/ PY - 2009/1/30/entrez PY - 2009/1/30/pubmed PY - 2009/3/3/medline SP - 122 EP - 30 JF - Pathophysiology of haemostasis and thrombosis JO - Pathophysiol Haemost Thromb VL - 36 IS - 3-4 N2 - Blood coagulation appears to play an important role in the occurrence of cancer and its effects may be twofold. First, in patients with cancer, blood coagulation is activated in the direction of a prothrombotic state. Second, a procoagulant environment may promote cancer in different ways. In this chapter we discuss some of the mechanisms that may be involved in this interplay between coagulation and cancer. Blood coagulation proteins interact with cells in the vasculature to maintain hemostasis. However, many proteins that are involved in coagulation and anticoagulation, as well as fibrinolysis, are also found in extravascular tissues. In different organs, these proteins may be involved in cell-signaling mechanisms, through interaction with cell receptors like protease-activated receptors (PARs). Such interactions may drive inflammation, angiogenesis and cell proliferation. The potential procarcinogenic actions of proteases like thrombin may be counteracted by the anticoagulant and anti-inflammatory actions of the protein C-thrombomodulin mechanism. In the blood of cancer patients, the balance is usually shifted towards a procoagulant direction. The resulting excess thrombin- and fibrin-forming activity promotes venous thrombosis and may in the extravascular compartment stimulate cancer progression. The activation of platelets and their interaction with leukocytes may propagate this process. In addition to the therapeutic modulation of the prothrombotic environment, the induction of specific anticoagulant proteins including thrombomodulin may have effects on tumor growth or dissemination, but the nature of these effects still remains hard to predict. The interplay between cancer and blood coagulation merits further experimental and clinical research. SN - 1424-8840 UR - https://www.unboundmedicine.com/medline/citation/19176985/Overview_of_the_postulated_mechanisms_linking_cancer_and_thrombosis_ L2 - https://www.karger.com?DOI=10.1159/000175150 DB - PRIME DP - Unbound Medicine ER -